紫草素对四氯化碳诱导的肝纤维化大鼠TGF-β1的影响
投稿时间:2018-03-15  修订日期:2018-05-10  点此下载全文
引用本文:鲁明霞,王红岗,胡仁标.紫草素对四氯化碳诱导的肝纤维化大鼠TGF-β1的影响[J].药学实践杂志,2018,36(5):453~456
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作者单位
鲁明霞 金华市人民医院, 浙江 金华 321000 
王红岗 金华市人民医院, 浙江 金华 321000 
胡仁标 宁德市人民医院, 福建 宁德 352000 
中文摘要:目的 观察紫草素对肝纤维化大鼠肝组织病理学改变及转化生长因子-β1(TGF-β1)含量的影响,探讨其对四氯化碳诱导的肝纤维化大鼠抗肝纤维化作用及可能的机制。方法 将40只SD大鼠随机分为空白组、模型组、阳性对照组、紫草素组。除空白组外,各组大鼠腹腔注射40%四氯化碳橄榄油溶液建立肝纤维化模型。造模同时,空白组与模型组予蒸馏水灌胃,阳性对照组予复方鳖甲软肝片水溶液灌胃,紫草素组予腹腔注射紫草素溶液,共干预10周。观察肝组织病理学变化;采用ELISA法测定层粘连蛋白、Ⅲ型前胶原含量,采用全自动生化仪分析ALT、AST含量,免疫组织化学法检测纤维化肝组织中TGF-β1的表达。结果 与空白组比较,模型组可见明显肝纤维化病理改变,AST、ALT水平升高(P<0.05),层粘连蛋白、Ⅲ型前胶原含量增高(P<0.05);与模型组比较,紫草素组肝纤维化程度较轻,血清ALT、ALT水平较低(P<0.05),层粘连蛋白、Ⅲ型前胶原含量下降(P<0.05),肝组织TGF-β1含量下降(P<0.05);与阳性对照组比较,紫草素组肝组织TGF-β1含量下降(P<0.05)。结论 紫草提取物紫草素可通过下调四氯化碳诱导的肝纤维化大鼠肝组织中TGF-β1的表达,从而抑制大鼠肝纤维化。
中文关键词:紫草素  肝纤维化  转化生长因子-β1
 
Effect of shikonin on expression of TGF-β1 in liver fibrosis induced by CCl4 in rats
Abstract:Objective To observe the influence of shikonin on pathological changes of liver tissue, expression of TGF-β1 in liver fibrosis in rats and to explore the possible mechanism of shikonin on rats' liver fibrosis. Methods 40 SD rats were randomly divided into four groups:normal group,model group,positive controlled group and shikonin group. Except normal group, the liver fibrosis models were introduced by subcutaneously injecting CCl4. Meanwhile, The normal group and the model group were intragastrically given the distilled water. The positive controlled group was intragastrically given Compound Biejiaruangan Troche solution. The treatments lasted for ten weeks. After treatments, pathological changes were observed. The alanine aminotransferase (ALT) and aspartate aminotransferase (AST)of serum were determined by automatic biochemical analyzer. The serum contents of laminin, procollagen type Ⅲ were assayed by ELISA. Transforming growth factor beta 1 (TGF-β1) index level was determined by immunohistochemistry. Results Compared with the normal group, liver fibrosis was detected in the model group. The serum levels of ALT,AST and the serum contents of laminin and procollagen type Ⅲ in the model group were significantly increased (P<0.05). Compared with the model group, the degree of liver fibrosis was less severe in shikonin group. The serum levels of ALT, AST, laminin, procollagen type Ⅲ and the expression of TGF-β1 in liver tissue were all decreased(P<0.05)in shikonin group. Compared with the positive controlled group, the expression of TGF-β1 in liver tissue was reduced in the shikonin group(P<0.05). Conclusion In SD rats, shikonin could inhibit the rats liver fibrosis induced with CCl4 by accommodating TGF-β1 expression in liver tissue.
keywords:shikonin  liver fibrosis  TGF-β1
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